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Dr. Carina Kern — CEO, LinkGevity — Necrosis Inhibitors To Pause The Diseases Of Aging

Necrosis Inhibitors To Pause The Diseases Of Aging — Dr. Carina Kern Ph.D. — CEO, LinkGevity

Dr. Carina Kern, Ph.D. is the CEO of LinkGevity (https://www.linkgevity.com/), an AI-powered biotech company driving innovation in drug discovery for aging and resilience loss.

Dr. Kern has developed a new Blueprint Theory of Aging, which takes an integrative approach to understanding aging, combining evolutionary theory, genetics, molecular mechanisms and medicine, and is used to structure LinkGevity’s AI.

Dr. Kern’s labs are based at the Babraham Research Campus, affiliated with the University of Cambridge and her research has led to the development of a first-in-class necrosis inhibitor targeting cellular degeneration (Anti-Necrotic™). This novel therapeutic is ready to begin Phase II clinical trials later this year, as a potential breakthrough treatment for aging, with UK Government, Francis Crick Institute KQ labs, and European Union (Horizon) support.

The Anti-Necrotic™ has also been selected as one of only 12 global innovations for NASA’s Space-Health program, recognizing its potential to mitigate accelerated aging in astronauts on long-duration space missions.

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DNA Methylation Signatures of Systemic Inflammation Are Associated With Brain Volume, Cognitive Trajectories, and Long‐Term Dementia Risk

Despite known links between inflammation and pathological aging outcomes, studies have found inconsistent associations between peripheral levels of inflammatory proteins, including CRP and GDF15, and markers of brain health and neurodegenerative disease (Dik et al. 2005 ; Ravaglia et al. 2007 ; Stevenson et al. 2020 ; Yang et al. 2015). A driver of these inconsistencies may be natural inter-and intra-day fluctuations and variability in plasma protein levels as well as potential measurement error (Conole et al. 2021 ; Moldoveanu et al. 2000 ; Stevenson et al. 2021). Moreover, many health conditions, as well as physical and psychological stressors, can cause transient changes in inflammatory proteins that may further contribute to variability in inflammatory protein abundance. A consequence of this variability is a difficulty in accurately estimating an individual’s long-term exposure to inflammatory stimuli, i.e., chronic inflammation. Alternatively, chronic inflammation can be measured by quantifying epigenetic signatures (DNA-methylation [DNAm]), which may act as determinants of inflammatory gene transcription (Gadd et al. 2022, 2024 ; Stevenson et al. 2021). Because DNAm, though modifiable, is more stable and less sensitive to inter-and intra-day fluctuations than circulating protein levels and is trained on the inputs of protein-DNAm associations from a large (13,399) number of individuals (Lu et al. 2022 ; Stevenson et al. 2020), blood-based DNAm scores can be derived to estimate one’s long-term exposure to a given protein.

Previously, DNAm measures of GDF15 and CRP have been used as a component of composite variables (e.g., GrimAge version 2) to capture the immunologic contributions to accelerated biological aging, morbidity, and mortality. DNAm CRP has been associated with adverse neurocognitive outcomes (Conole et al. 2021 ; Smith et al. 2024). Specifically, Conole and colleagues found that DNAm CRP was significantly associated with cross-sectional brain atrophy, white matter microstructure, and cognitive performance, and that epigenetic CRP measures were more strongly associated with measures of brain structure than were circulating CRP protein levels. Similarly, Smith et al. (2024) found that elevated DNAm CRP was cross-sectionally associated with lower MRI-defined brain volume, as well as greater dementia risk over a 16-year follow-up period (Smith et al. 2024). Although higher levels of GDF15 protein have also been linked to poor brain health and dementia risk (Isik et al. 2024 ; Walker et al. 2024 ; Walker, Chen, et al. 2023), less is known about the extent to which an epigenetic indicator of long-term GDF15 exposure (DNAm GDF15) relates to adverse neurocognitive outcomes (Gadd et al. 2024).

The current study examined DNAm measures of CRP and GDF15—two inflammatory proteins with distinct immunologic significance—and extended previous cross-sectional findings using longitudinal MRI imaging and cognitive data in a large cohort of Baltimore Longitudinal Study of Aging (BLSA) adults. We conducted a proteome-wide analysis to identify functional pathways associated with blood DNAm CRP and DNAm GDF15 scores and examined how each of these putative markers of chronic inflammation was associated with longitudinal measures of brain structure as well as cognitive function among older adults. Additionally, we compared the performance of the CRP and GDF15 DNAm scores to that of their plasma protein counterparts and determined whether the DNAm associations extended to near-and long-term dementia risk in two independent cohort studies.

If We Escape All Major Diseases, Neurodegeneration And Respiratory Failure Is Likely

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The Waist-To-Hip RatioModifies LP(a)-Associated CVD Risk

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Use Code: CONQUERAGING At Checkout.

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Unlocking the genome’s hidden half with new DNA sequencing technology

Cornell researchers have found that a new DNA sequencing technology can be used to study how transposons move within and bind to the genome. Transposons play critical roles in immune response, neurological function and genetic evolution, and implications of the finding include agricultural advancements and understanding disease development and treatment.

In a paper published in iScience, senior author Patrick Murphy, Ph.D. ‘13, associate professor of molecular biology and genetics in the College of Agriculture and Life Sciences, and co-authors demonstrate that a high-resolution genome mapping technique called CUT&Tag can overcome shortcomings in existing sequencing methods to enable study of transposons.

Once derided as “junk DNA,” transposons make up half the human genome and are descended from ancient viruses encountered by our evolutionary ancestors.

Genetic engineering reduces plant’s chromosome number without affecting its growth

Higher yields, greater resilience to climatic changes or diseases—the demands on crop plants are constantly growing. To address these challenges, researchers of Karlsruhe Institute of Technology (KIT) are developing new methods in genetic engineering.

In cooperation with other German and Czech researchers, they succeeded for the first time in leveraging the CRISPR/Cas molecular scissors for changing the number of chromosomes in the Arabidopsis thaliana model organism in a targeted way—without any adverse effects on plant growth. This discovery opens up new perspectives for plant breeding and agriculture. The results have been published in Science.

The CRISPR/Cas molecular scissors enabled the KIT researchers in recent years to alter not only genes, but also chromosomes. This way, it is possible to combine wanted traits or eliminate unwanted ones in plants in a targeted manner.

Cortical GABAergic projection neurons are implicated in schizophrenia

Schizophrenia stems from abnormal brain development, which can begin even before birth. Yet symptoms typically don’t appear until later in life.

“For a long time, the brain is able to compensate for developmental errors and maintain relatively normal function. But at some point, it’s like a chain snapping — the brain can no longer compensate, and that’s when symptoms emerge. Until that point, however, prevention should be possible,” says one of the study’s first authors.

They investigated when this turning point occurs. By tracking brain development from the fetal stage to adulthood, they found that dramatic changes happen late in the brain’s development. Up until the transition from childhood to adolescence, molecular and functional changes in the brain were rather minor, likely explaining lack of symptoms before adolescence.

The researchers have worked with mice carrying a specific genetic mutation known as “15q13.3 microdeletion syndrome.” In humans, this syndrome is associated with epilepsy, schizophrenia, autism, and other neurodevelopmental disorders.

“We know that sleep is often disrupted in people with psychiatric disorders, so we chose to use sleep as a behavioral marker—something we could observe. We examined both the mice’s behavior and the activity of a specific type of brain cell. Our findings show that one particular cell type (γ-aminobutyric acid (GABAergic) projecting neurons) is significantly affected in the test animals compared to healthy mice,” explains the author.

These GABAergic rare brain cells are often overlooked because they make up only a tiny fraction of the brain’s total cell population. Nevertheless, they play a crucial role in regulating many brain functions.

The new study not only demonstrates a link between this specific type of brain cell and sleep — it also shows that the mice’s sleep patterns began to resemble those of healthy mice when researchers reduced the activity of the cell type in question.

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